How to Reverse Testicular Atrophy

Free Methods On How To Get Bigger Testicles. Download the free ebook today to start to see rapid boosts in testicular performance and size within 2 or 3 days. Inside, youll learn: A cutting edge sexual technique to get instantly bigger testes after lovemaking. An unusual tip to fire up your testicles and increase your ejaculations within a week. A subliminal trick to restore morning wood and get your sack feeling heavy in the morning. How to avoid for Good this nasty chemical found in food and normal substances that causes testicular atrophy in men. Elevated estrogen is the leading cause of testicular atrophy in human males. So you need to keep estrogen levels in check if you want to avoid this testicular shrinkage and weak libido. A simple way to do this is to eat cruciferous veggies like broccoli, cabbage and Brussels sprouts Because these vegetables contain phytonutrients that flush bad estrogens out of your body. The most potent of these is Diindolymethane. Take in just enough of this nutrient and your testicles will be protected. But if you take in too much youll actually increase the aromatase enzyme in your body. Because Mark is a pro researcher on testosterone, testicular function and male fertility, so he will reveal the hard facts. But he also explains to you exactly how to reverse the whole process in just a few weeks. Read more here...

Hypogastric plexus block is useful in relieving visceral pain due to cancer from the descending colon, sigmoid colon, and rectum. It is also useful in pain originating from cancer of the bladder, prostatic urethra, prostate, seminal vesicles, and testicles. Pain from the cancer of the uterus, ovary, and vaginal fundus also can be treated with hypogastric plexus block. The efficacy of neurolytic block depends on the location and extent of the tumor. It is overall considered as a good adjuvant to pain management in cancer pain from the lower GI tract and pelvic organs. The goal is to eliminate the pain or decrease it, so that concomitant oral opioid administration can control the pain without significant side effects.

Estimates of levels of exposure to boron posing minimal risk to humans (MRLs) have been made. These are discussed in Section 2.2 and were based on data believed to be reliable for the most sensitive noncancer effect for each route and exposure duration. No data were located on effects of acute-duration inhalation exposure in humans or animals nor on intermediate-duration inhalation exposure to boron in humans. Available information on intermediate-duration inhalation exposure in animals and chronic-duration inhalation exposure in humans do not reliably identify the most sensitive target organ. No data on effects of acute-duration oral exposure to boron in humans or animals nor on intermediate exposure in humans were located. In animals, prenatal exposure of mice (79 mg boron kg day as boric acid) and rats (13.6 mg boron kg day as boric acid) during gestation days 0-17 and 0-20 caused developmental effects consisting of reduced fetal body weight or minor skeletal changes and possibly...

Immunocytochemical as well as in situ hybridization studies demonstrate that GCPII is selectively expressed in astrocytes in the brain with an uneven regional distribution.38, 39 Particularly high levels of expression are observed in the Bergmann glial cells. It is also expressed in non-myelating Schwann cells in the periphery, including those surrounding motor neuron terminals at the end plate.40 In the periphery, GCPII is expressed in the testicles and in the tubules of the kidney. However, the exclusive role of GCPII in the hydrolysis of NAAG has been called into question by studies in mice homozygous for a null mutation of the GCPII gene. The brains of these mice exhibit a residual of 15 GCPII-like enzyme activity with no alterations observed in the levels of NAAG, NAA, glutamate or aspartate.41 Recently, a second gene with high homology to GCPII has been cloned.42, 43

Survival was also reduced in mice following intermediate-duration exposure. Males (10 ) died after exposure to a dose of 288 mg boron kg day (as boric acid) in the diet, while 80 of males and 60 of females died at 577 mg boron kg day (NTP 1987). Hyperkeratosis and or acanthosis in the stomach and extramedullary hematopoiesis of the spleen in both sexes were observed at the highest dose tested (577 mg boron kg day). There was 100 mortality in rats fed 263 mg boron kg day for 90 days (Weir and Fisher 1972). Congestion of liver and kidneys, small gonads, and brain swelling were reported. When male mice consumed 48 and 96 mg boron kg day (as boric acid) for 103 weeks, mortality was 40 and 56 , respectively, compared to 18 in untreated controls (NTP 1987). No clinical signs were reported however, boron caused increased incidence of testicular atrophy and interstitial hyperplasia. Mortality in female mice was 30 and 24 (48 and 96 mg boron kg day) compared to 34 in the untreated controls...

Neurological damage has been reported in humans. Neurological effects reported in humans have focused primarily on histopathological alterations. No data were provided on biochemical changes. In animals, testicular atrophy and reduced sperm production have been demonstrated following chronic boron exposure. There are clinical and biochemical tests to detect neurological and gonadal injury, but these are not specific for boron exposure. Sparse data in animals suggest some biochemical changes for instance, cerebral succinate dehydrogenase was increased in rats after boron exposure. Animal data further demonstrate biochemical alterations following gonadal injury. Dose-dependent reduction in hyaluronidase, sorbitol dehydrogenase, and lactic acid dehydrogenase (isoenzyme-X) were observed in rats following boron exposure.

Recent publications demonstrate that perinatal exposure to a number of phthalate esters alters development of the male reproductive tract in an antian-drogenic manner, causing underdevelopment and agenesis of the epididymis at relative low dosage levels. Arcardi et al. 165 reported that administration of DEHP in the drinking water to the dam during pregnancy and lactation (estimated LOAEL of 3 mg kg day) produced testicular histopathological alterations in male rat offspring. Although DEHP is not an AR antagonist in vitro at concentrations up to 10 imol l, it inhibits fetal Leydig cell testosterone synthesis in vivo when orally administered to the dam at 0.75 g kg day starting at day 14 of pregnancy. As a consequence, fetal testosterone concentrations are reduced in males to female levels from day 17 of gestation to 2 days after birth. This reduction in testosterone levels results in a wide range of malformations of the androgen-dependent tissues in male rats including reduced AGD,...

Northern blot studies of GalR3 mRNA initially showed that GalR3 mRNA is present in the heart, spleen, and testis (Wang et al. 1997a). Later, with the help of more sensitive methods, GalR3 transcripts were also detected in the CNS, with the highest levels in the hypothalamus and pituitary. Other regions, like the olfactory bulb, cerebral cortex, medulla oblongata, caudate putamen, cerebellum, and spinal cord, but not the hippocampus and substantia nigra, were also found to contain GalR3 mRNA (Smith et al. 1998). In the periphery, GalR3 mRNA is widespread, with existence in the liver, kidney, stomach, testicles, adrenal cortex,